Abstract:
Mulberry leaf alkaloids (MLA) were tested for their ability to ameliorate alcoholic liver injury (ALI) in a mouse model of the disease. First, ALI was induced in mice, following which the animals were treated with one of three different doses of MLA (40, 80, and 160 mg/kg•day) for four weeks. Then, the serum levels of triglyceride (TG), total cholesterol (TC), alanine aminotransferase (ALT), and aspartate aminotransferase (AST); enzymatic activities of liver catalase (CAT), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD); and liver levels of malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), and interleukin-6 (IL-6) were measured. Compared with the values from the control group, the liver index; serum levels of TG, TC, ALT, and AST; and MDA, IL-1β, IL-6, and TNF-α levels of the group treated with middle-dose MLA were lower by 11.18%, 22.78%, 19.19%, 28.08%, 16.16%, 25.07%, 23.51%, 18.61%, and 11.78%, respectively. By contrast, the liver SOD, CAT, and GSH-Px activities of the middle-dose MLA group were higher by 27.47%, 15.36%, and 27.83% respectively. In the high-dose MLA group, the liver index; serum levels of TG, TC, ALT, and AST; and liver levels of MDA, IL-1β, IL-6, and TNF-α were lower by 15.17%, 32.65%, 23.16%, 30.58%, 16.41%, 31.97%, 27.19%, 25.41%, and 29.59%, respectively, than the levels in the control group; however, the liver SOD, CAT, and GSH-Px activities were higher by 38.38%, 19.09%, and 31.09%, respectively. The structural damage to the liver tissue was significantly ameliorated in the medium- and high-dose MLA groups. In summary, MLA can ameliorate alcoholic liver injury in mice, with the possible mechanism being related to its actions in alleviating liver oxidative stress and inhibiting the inflammatory response.
